炎症因子IL-6的效应信号通路及下游STAT3的磷酸化活化在炎症启动和进展中发挥关键作用，其效应信号通路的调控机制是炎症研究领域中重要的前沿科学问题。RIG-I是胞内病毒RNA的识别受体，在抗病毒天然免疫应答中发挥关键作用。但是，RIG-I是否对炎症因子效应信号通路尤其是IL-6效应通路具有调控作用目前未知。申请人前期报道了RIG-I在干扰素效应信号通路中的调控作用和机制，以排名第一发表于Cancer Cell（2014,25:49-63）（IF:23.5）。同时我们发现，在RIG-I敲除小鼠中，IL-6效应信号通路及下游STAT3的磷酸化活化显著增强。据此，本工作拟进一步研究RIG-I调控IL-6的效应信号通路尤其是STAT3磷酸化活化的作用和机制，并结合肝脏炎症小鼠疾病模型，探求RIG-I在肝脏炎症疾病进展中的作用及其作为干预靶点和预警指标的价值，以期为肝脏炎症提出新机制和干预新思路。

Inflammatory cytokine IL-6 effector signaling and downstream activation of STAT3 play important roles in the initiation and progression of inflammation. The regulatory mechanism of IL-6 effector signaling is an important question in the research of innate immunity. RIG-I is an intracellular sensor of viral RNA and play critical roles in host antiviral innate immune response. However, the roles of RIG-I in the regulation of inflammatory cytokines effector signaling, especially in IL-6 effector signaling, remain elusive up to now. We previously reported the RIG-I promoted interferon effector signaling, which was published in Cancer Cell (2014, 25: 49-63) (IF: 23.5) as the first author. Also, we found that IL-6 effector signaling and STAT3 activation were significantly enhanced in RIG-I knockout mice. Hence, we intend to investigate the roles of RIG-I in the regulation of IL-6 effector signaling, especially STAT3 phosphorylation and activation. Moreover, we intend to investigate the roles of RIG-I in the liver inflammatory mouse disease models, so as to suggest new mechanisms and therapeutic targets for liver inflammation.